DAMS Question Bank 2019th Edition Unknown

install download

https://ebookmeta.com/product/dams-question-bank-2019th-edition-
unknown/

Download more ebook from https://ebookmeta.com

We believe these products will be a great fit for you. Click
the link to download now, or visit ebookmeta.com
to discover even more!

SSMC Question Bank 50th Edition Myedul Islam Naem

https://ebookmeta.com/product/ssmc-question-bank-50th-edition-
myedul-islam-naem/

KV SCIENCE QUESTION BANK 2022 23 1st Edition Kv

https://ebookmeta.com/product/kv-science-question-
bank-2022-23-1st-edition-kv/

ISC Class 12 Oswaal Chemistry Question Bank 1st Edition

Oswaal Editorial Board

https://ebookmeta.com/product/isc-class-12-oswaal-chemistry-
question-bank-1st-edition-oswaal-editorial-board/

Narrative Being Vs Narrating Being 1st Edition Armela

Panajoti

https://ebookmeta.com/product/narrative-being-vs-narrating-
being-1st-edition-armela-panajoti/
An Introduction to Mathematical Cognition 1st Edition
Camilla Gilmore

https://ebookmeta.com/product/an-introduction-to-mathematical-
cognition-1st-edition-camilla-gilmore/

Colour in Art World of Art 2nd Edition John Gage

https://ebookmeta.com/product/colour-in-art-world-of-art-2nd-
edition-john-gage/

Meta analysis in Clinical Research Principles and

Procedures Anoop Kumar

https://ebookmeta.com/product/meta-analysis-in-clinical-research-
principles-and-procedures-anoop-kumar-2/

Action Sports and the Olympic Games Past Present Future

1st Edition Belinda Wheaton

https://ebookmeta.com/product/action-sports-and-the-olympic-
games-past-present-future-1st-edition-belinda-wheaton/

Court of Ice and Ash 1st Edition L J Andrews

https://ebookmeta.com/product/court-of-ice-and-ash-1st-edition-l-
j-andrews/
Practical Guide to Shifting Realities Unknown

https://ebookmeta.com/product/practical-guide-to-shifting-
realities-unknown/
 DAMS QUESTION BANK–II
DQB-II
PARACLINICALS
1. PATHOLOGY
2. PHARMACOLOGY
3. MICROBIOLOGY
4. FORENSIC MEDICINE &
TOXICOLOGY

For PG Medical Entrance

Published by Delhi Academy of Medical Sciences (P)
Ltd.

HEAD OFFICE
Delhi Academy of Medical Sciences (P.) Ltd.
4-B, Grovers Chamber, Pusa Road,
Near Karol Bagh Metro Station,
New Delhi-110 005
Phone : 011-4009 4009
http://www.damsdelhi.com
Email: info@damsdelhi.com

ISBN : 978-93-87503-75-5

First Published 1999, Delhi Academy of Medical Sciences

© 2019 DAMS Publications

All rights reserved. No part of this book may be reproduced

or transmitted in any form or by any means, electronic,
mechanical, including photocopying, recording, or any
information storage and retrieval system without
permission, in writing, from the author and the publishers.
This book contains information obtained from authentic and
highly regarded sources. Reprinted material is quoted with
permission. Reasonable efforts have been made to publish
reliable data and information, but the authors and the
publishers cannot assume responsibility for the validity of all
materials. Neither the authors nor the publishers, nor
anyone else associated with this publication, shall be liable
for any loss, damage or liability directly or indirectly caused
or alleged to be caused by this book.
Neither this book nor any part may be reproduced or
transmitted in any form or by any means, electronic or
mechanical, including photocopying, microfilming and
recording, or by any information storage or retrieval system,
without permission in writing from Delhi Academy of
Medical Sciences. The consent of Delhi Academy of Medical
Sciences does not extend to copying for general distribution,
for promotion, for creating new works, or for resale. Specific
permission must be obtained in writing from Delhi Academy
of Medical Sciences for such copying.
Trademark notice: Product or corporate names may be
trademarks or registered trademarks, and are used only for
identification and explanation, without intent to infringe.
Typeset by Delhi Academy of Medical Sciences Pvt. Ltd., New
Delhi (India).
 Contents

1. PATHOLOGY
Q1 Cell as a Unit of Health and Disease – Questions
A1 Cell as a Unit of Health and Disease – Explanations
Q2 Cell Adaptation, Injury and Death – Questions
A2 Cell Adaptation, Injury and Death – Explanations
Q3 Inflammation, Repair and Hemodynamics – Questions
A3 Inflammation, Repair and Hemodynamics – Explanations
Q4 Genetics – Questions
A4 Genetics – Explanations
Q5 Diseases of the Immune System – Questions
A5 Diseases of the Immune System – Explanations
Q6 Neoplasia – Questions
A6 Neoplasia – Explanations
Q7 Red Blood Cells and its Disorders – Questions
A7 Red Blood Cells and its Disorders – Explanations
Q8 WBC Disorders – Questions
A8 WBC Disorders – Explanations
Q9 Platelet Disorders – Questions
A9 Platelet Disorders – Explanations
Q10 Transfusion Medicine – Questions
A10 Transfusion Medicine – Explanations
Q11 Systemic Pathology – Questions
A11 Systemic Pathology – Explanations

2. PHARMACOLOGY
Q1 General Pharmacology — Questions
A1 General Pharmacology — Explanations
Q2 Autonomic Nervous System — Questions
A2 Autonomic Nervous System — Explanations
Q3 Autacoids — Questions
A3 Autacoids — Explanations
Q4 Respiratory System — Questions
A4 Respiratory System — Explanations
Q5 Endocrine System — Questions
A5 Endocrine System — Explanations
Q6 Anaesthesia — Questions
A6 Anaesthesia — Explanations
Q7 Central Nervous System — Questions
A7 Central Nervous System — Explanations
Q8 Cardiovascular System — Questions
A8 Cardiovascular System — Explanations
Q9 Hematology — Questions
A9 Hematology — Explanations
Q10 Gastrointestinal System — Questions
A10 Gastrointestinal System — Explanations
Q11 Antimicrobial Drugs — Questions
A11 Antimicrobial Drugs — Explanations

3. MICROBIOLOGY
Q1 General Microbiology — Questions
A1 General Microbiology — Explanations
Q2 Immunology — Questions
A2 Immunology – Explanations
Q3 Bacteriology — Questions
A3 Bacteriology — Explanations
Q4 Virology — Questions
A4 Virology — Explanations
Q5 Mycology — Questions
A5 Mycology — Explanations
Q6 Parasitology — Questions
A6 Parasitology — Explanations

4. FORENSIC MEDICINE & TOXICOLOGY

Q Questions
A Explanations
 Cell as a Unit of Health and Disease –
Questions
1. Which of the following plays a role in gene editing?
a. Gene Xpert
b. CRISPR
c. Heath care apps
d. Big data

2. Cell to cell permeability occurs through:

a. Occludin
b. Zona adherens
c. Connexins
d. Zonulin

3. Which Collagen is typical of basement membrane?

a. Type I
b. Type II
c. Type III
d. Type IV

4. All of the following are Intermediate filament except?

a. Lamin
b. Cadherin
c. Vimentin
d. Desmin

5. Titin protein mutated in?

a. DCM
b. HOCM
c. RCM
d. Non-functional cardiomyopathy

6. Bridging fibrosis in large wounds is due to:

a. Keratinocyte growth factor
b. Epidermal growth factor
c. Platelet derived growth factor
d. Transforming growth factor-β

7. Types of collage playing important role in wound healing

a. I and III
b. II and V
c. III and IV
d. V and IX
8. Oval stem cells are located in-
a. Canal of schlemm
b. Canal of herring
c. Space of disse
d. Basal lamina of myotubules

9. Heritable changes in gene expression not caused by alterations in DNA

sequence refers to?
a. Genetics
b. Epigenetics
c. Mutations
d. Transposons

10. Epigenetic factors refers to?

a. Histone methylation
b. Histone phosphorylation
c. DNA methylation
d. All of the above

11. Collagen present in cornea?

a. Type 1
b. Type 2
c. Type 4
d. Type 7

12. Gene silencing RNA-

a. rRNA
b. tRNA
c. miRNA
d. None

13. The most abundant glycoprotein present in basement membrane is-

a. Laminin
b. Fibronectin
c. Collagen type 4
d. Heparan sulphate

1. b 2. c 3. d 4. b 5. a 6. d 7. a 8. b 9. b 10. d 11. b

12. c 13. a

14. Which of the following statement is not true?

a. Cytokeratin is the marker of muscle cells
b. Vimentin is used to stain fibroblasts
c. Neurofilaments are present in neurons
d. Desmin can be used as a marker for muscle cells
15. Which of the following is both morphogenic and mitogenic?
a. Insulin growth factor
b. Bone morphogenic factor
c. Fibroblast growth factor
d. Epidermal growth factor

16. Which of the following is involved in stem cell self renewal and
pluripotency?
a. Oct 3/4
b. sox 2
c. c-myc
d. FLT3 ligand
e. c-kit

17. All of the following are true about single nucleotide polymorphisms except
a. Almost always biallelic
b. 1% occur in non coding regions
c. Can be neutral variant with no effect on gene function
d. Can serve as a marker for disease

18. Which of the following statements is true?

a. Actin is the most abundant cytosolic protein in the cell
b. Lamin is the most abundant glycoprotein in the basement membrane
c. Fibronectin imparts scaffolding to the cytoplasm
d. FACITs are seen in association with type I collagen

19. Which of the following pairs of cell cycle phase and cyclin/CDK is
incorrectly matched?
a. G1S checkpoint- cyclin D/CDK 6
b. G1S checkpoint- cyclin D/CDK4
c. S phase- cyclin A/CDK 6
d. G2M checkpoint- cyclin B/CDK1

20. Which of the following organ and site of stem cell is incorrectly matched?
a. Liver- oval cells in Space of Disse
b. Skin- bulge of hair follicle
c. Brain- dentate gyrus
d. Cornea- limbus

21. Major cytokine involved in fibrosis

a. Transforming growth factor-α
b. Transforming growth factor-β
c. Fibroblast growth factor
d. Epidermal growth factor

22. Most abundant collagen in the body?

 a. Type I
b. Type II
c. Type III
d. Type IV

23. FACIT collagen is?

a. Type I
b. Type III
c. Type IX
d. Type XI

14. a 15. b 16. a, 17. b 18. a 19. c 20. a 21. b 22. a 23. c
b, c, e
 Cell as a Unit of Health and Disease –
Explanations
1. B
Reference: Robbins Basic Pathology, 10th Edition
Clustered regularly interspaced short palindromic repeats (CRISPRs) and Cas (or
CRISPRassociated genes) are linked genetic elements that endow prokaryotes with a
form of acquired immunity to phages and plasmids. Bacteria use this system to
sample the DNA of infecting agents, incorporating it into the host genome as CRISPRs.
CRISPRs are transcribed and processed into an RNA sequence that binds and directs
the nuclease Cas9 to a sequences (e.g., a phage), leading to its cleavage and the
destruction of the phage. Gene editing repurposes this process by using artificial
guide RNAs (gRNAs) that bind Cas9 and are complementary to a DNA sequence of
interest. Once directed to the target sequence by the gRNA, Cas9 induces double-
strand DNA breaks.
Option A- The Xpert MTB/RIF is a cartridge-based nucleic acid amplification test for
simultaneous rapid tuberculosis diagnosis and rapid antibiotic sensitivity test. It is an
automated diagnostic test that can identify Mycobacterium tuberculosis DNA and
resistance to rifampicin
Option C and Option D are far removed from gene editing and have no bearing
whatsoever to Genomics

2. C
Reference: Robbins Pathological Basis of Disease, 9th edition
Communicating junctions (gap junctions) mediate the passage of chemical or
electrical signals from one cell to another. The junction consists of a dense planar array
of 1.5- to 2-nm pores (called connexons) formed by hexamers of transmembrane
protein connexins. These pores permit the passage of ions, nucleotides, sugars, amino
acids, vitamins, and other small molecules; the permeability of the junction is rapidly
reduced by lowered intracellular pH or increased intracellular calcium.
Option A and D- Occluding junctions (tight junctions) seal adjacent cells together to
create a continuous barrier that restricts the paracellular (between cells) movement of
ions and other molecules. Viewed en face, occluding junctions form a tight meshlike
network of macromolecular contacts between neighboring cells. The complexes that
mediate these cell–cell interactions are composed of multiple proteins, including
occludin, claudin, zonulin, and catenin
Option B- When the adhesion focus is between cells, and is small and rivet-like, it is
designated a spot desmosome or macula adherens. When such a focus attaches the
cell to the ECM, it is called a hemidesmosome. Similar adhesion domains can also
occur as broad bands between cells, where they are denoted as belt desmosomes or
zona adherens.

3. D
Reference: Robbins Pathological Basis of Disease, 9th edition
Non-fibrillar collagens may contribute to the structures of planar basement
membranes (type IV collagen).

4. B
 Intermediate filaments are 10-nm diameter fibrils that comprise a large and
heterogeneous family. Individual types have characteristic tissue-specific patterns of
expression that can be useful for assigning a cell of origin for poorly differentiated
tumors.
Lamin A, B, and C: nuclear lamina of all cells
Vimentin: mesenchymal cells (fibroblasts, endothelium)
Desmin: muscle cells, forming the scaffold on which actin and myosin contract
Neurofilaments: axons of neurons, imparting strength and rigidity
Glial fibrillary acidic protein: glial cells around neurons
Cytokeratins: at least 30 distinct varieties, subdivided into acidic (type I) and
neutral/basic (type II); different types present in different cells, hence can be used as
cell markers
Option A and D- Intermediate filaments
Option B- Cell-cell desmosomal junctions are formed by homotypic association of
transmembrane glycoproteins called cadherins

5. A
Reference: Robbins Pathological Basis of Disease, 9th edition
DCM is familial in at least 30% to 50% of cases, in which it is caused by mutations in a
diverse group of more than 20 genes encoding proteins involved in the cytoskeleton,
sarcolemma, and nuclear envelope (laminin A/C). In particular, mutations in TTN, a
gene that encodes titin (so-called because it is the largest protein expressed in
humans), may account for approximately 20% of all cases of DCM.
Option B- Mutations causing HCM are found most commonly in the gene encoding β-
myosin heavy chain (β-MHC), followed by the genes coding for cardiac TnT, α-
tropomyosin, and myosin-binding protein C (MYBP-C); overall, these account for 70%
to 80% of all cases.
Option C- Restrictive cardiomyopathy can be idiopathic or associated with distinct
diseases or processes that affect the myocardium, principally radiation fibrosis,
amyloidosis, sarcoidosis, metastatic tumors, or the deposition of metabolites that
accumulate due to inborn errors of metabolism.
Option D- It is a non specific terminology.

6. D
Reference: Robbins Pathological Basis of Disease, 9th edition
TGF-β drives scar formation, and applies brakes on the inflammation that accompanies
wound healing.
• TGF-β stimulates the production of collagen, fibronectin, and proteoglycans, and it
inhibits collagen degradation by both decreasing matrix metalloproteinase (MMP)
activity and increasing the activity of tissue inhibitors of proteinases. TGF-β is involved
not only in scar formation after injury, but also drives fibrosis in lung, liver, and
kidneys in the setting of chronic inflammation.
• TGF-β is an antiinflammatory cytokine that serves to limit and terminate
inflammatory responses. It does this by inhibiting lymphocyte proliferation and the
activity of other leukocytes. Animal models lacking TGF-β have widespread and
persistent inflammation
Option A, B and C- Refer to the following table

Growth Factor Sources Functions

Epidermal. growth Activated macrophages, Mitogenic for keratinocytes and fibroblasts; stimulates
factor (EGF) salivary glands, keratinocyte migration; stimulates formation of
keratinocytes, and many granulation tissue
other cells

Transforming growth Activated macrophages, Stimulates proliferation of hepatocytes and many other
factor-α (FGF-α) keratinocytes, many other epithelial cells
cell types

Hepatocyte growth Fibroblasts, stromal cells In Enhances proliferation of hepatocytes and other
factor (HGF) the liver, endothelial cells epithelial cells; Increases cell motility
(scatter factor)

Vascular endothelial Mesenchyme cells Stimulates proliferation of endothelial cells; Increases

growth factor vascular permeability
(VEGF}

Platelet-derived Platelets, macrophages, Chemotactic for neutrophils, macrophages, fibroblasts,

growth factor endothelial cells, smooth and smooth muscle cells; activates and stimulates
IPOGF) muscle cells, keratinocytes proliferation of fibroblasts, endothelial, and other cells;
stimulates ECM protein synthesis

Fibroblast growth Macrophages, mast cells, Chemotactic and mitogenic for fibroblasts; stimulates
factors (FGFs), endothelial cells, many other angiogenesis and ECM protein synthesis
Including acidic (FGF- cell types
1) and basic (FGF-2)

Transforming growth Platelets, T lymphocytes, Chemotactic for leukocytes and fibroblasts; stimulates
factor-β (TGF-β) macrophages, endothelial ECM protein synthesis; suppresses acute Inflammation
cells, keratinocytes, smooth
muscle cells, fibroblasts

Keratinocyte growth fibroblasts Stimulates keratinocyte migration, proliferation, and

factor (KGF) (i.e., differentiation
FGF-7)

ECM Extracellular membrane.

7. A
Reference: Robbins Pathological Basis of Disease, 9th edition
At first a provisional matrix containing fibrin, plasma fibronectin, and type III collagen
is formed, but in about 2 weeks this is replaced by a matrix composed primarily of
type I collagen. Ultimately, the original granulation tissue scaffold is converted into a
pale, avascular scar, composed of spindleshaped fibroblasts, dense collagen,
fragments of elastic tissue, and other ECM components

8. B
Reference: Robbins Pathological Basis of Disease, 9th edition
In situations where the proliferative capacity of hepatocytes is impaired, such as after
chronic liver injury or inflammation, progenitor cells in the liver contribute to
repopulation. In rodents, these progenitor cells have been called oval cells because of
the shape of their nuclei. Some of these progenitor cells reside in specialized niches
called canals of Hering, where bile canaliculi connect with larger bile ducts. The
signals that drive proliferation of progenitor cells and their differentiation into mature
hepatocytes are topics of active investigation.
Option A- circular lymphatic-like vessel in the eye that collects aqueous humor from
the anterior chamber and delivers it into the episcleral blood vessels via aqueous veins
 Option C- location in the liver between a hepatocyte and a sinusoid. It contains the
blood plasma. Microvilli of hepatocytes extend into this space, allowing proteins and
other plasma components from the sinusoids to be absorbed by the hepatocytes.
Fenestration and discontinuity of the endothelium, as well as its basement membrane,
facilitates this transport.
Option D- Site of regeneration

9. B
Option A- Genetics is the study of genes, genetic variation, and heredity in living
organism
Option C- A gene mutation is a permanent alteration in the DNA sequence
Option D- DNA sequence that can change its position within a genome, sometimes
creating or reversing mutations and altering the cell’s genetic identity and genome
size. Transposition often results in duplication of the same genetic material.

10. D
Epigenetic factors include-
Histone methylation
Histone phosphorylation
Histone acetylation
DNA methylation
Chromatin organising factors

11. B

COLLAGEN TYPE TISSUE DISTRIBUTION GENETIC DISORDERS

Fibrillar Collagens

I Ubiquitous in hard and soft tissues Osteogenesis Imperfecta

II Cartilage, intervertebral disc, vitreous Achondrogenesis type 2

III Hollow organs, soft tissues Vascular Ehler Danlos Syndrome

V Soft tissues, blood vessels Classical Ehler Danlos Syndrome

IX Cartilage, vitreous Stickler Syndrome

Basement Membrane Collagen

IV Basement membranes Alport Syndrome

12. C
Noncoding RNAs are encoded by genes that are transcribed but not translated.
Although many distinct families of noncoding RNAs exist, we will only discuss two
examples here: small RNA molecules called microRNAs, and long noncoding RNAs
>200 nucleotides in length. Post transcriptional silencing of gene expression by
miRNA is a fundamental and well-conserved mechanism of gene regulation present in
all eukaryotes (plants and animals).
Option A- ribosomal RNA Option B- transfer RNA

13. A
Prototypical adhesive glycoproteins include fibronectin (a major component of the
interstitial ECM) and laminin (a major constituent of basement membrane). Integrins
are representative of the adhesion receptors, also known as cell adhesion molecules
(CAMs); the CAMs also include immunoglobulins, cadherins, and selectins.
 Option A- Laminin is the most abundant glycoprotein in basement membrane. It is an
820-kD cross-shaped heterotrimer that connects cells to underlying ECM components
such as type IV collagen and heparan sulfate. Besides mediating attachment to
basement membrane, laminin can also modulate cell proliferation, differentiation, and
motility
Option B- Fibronectin is a large (450 kD) disulfide-linked heterodimer that exists in
tissue and plasma forms; it is synthesized by a variety of cells, including fibroblasts,
monocytes, and endothelium.
Option C- Basement membrane collagen
Option D- Proteoglycans form highly hydrated compressible gels that confer resistance
to compressive forces; in joint cartilage, proteoglycans also provide a layer of
lubrication between adjacent boney surfaces. Proteoglycans consist of long
polysaccharides, called glycosaminoglycans (examples are keratan sulfate and
chondroitin sulfate) attached to a core protein; these are then linked to a long
hyaluronic acid polymer called hyaluronan, in a manner reminiscent of the bristles on
a test tube brush.

14. A
Cytokeratin is a marker for epithelial cells
Option B- Vimentin is a marker for mesenchymal cells and tumors arising from them
Option C- stains axons of neurofilaments
Option D- stains muscle cells and tumors arising from them

15. B
Bone morphogenetic proteins (BMPs) are multi-functional growth factors that belong
to the transforming growth factor beta (TGFbeta) superfamily and are both
morphogenic and mitogenic.

Growth Factor Sources Functions

Epidermal. growth Activated macrophages, Mitogenic for keratinocytes and fibroblasts; stimulates
factor (EGF) salivary glands, keratinocyte migration; stimulates formation of
keratinocytes, and many granulation tissue
other cells

Transforming growth Activated macrophages, Stimulates proliferation of hepatocytes and many other
factor-α (FGF-α) keratinocytes, many other epithelial cells
cell types

Hepatocyte growth Fibroblasts, stromal cells In Enhances proliferation of hepatocytes and other
factor (HGF) the liver, endothelial cells epithelial cells; Increases cell motility
(scatter factor)

Vascular endothelial Mesenchyme cells Stimulates proliferation of endothelial cells; Increases

growth factor vascular permeability
(VEGF}

Platelet-derived Platelets, macrophages, Chemotactic for neutrophils, macrophages, fibroblasts,

growth factor endothelial cells, smooth and smooth muscle cells; activates and stimulates
IPOGF) muscle cells, keratinocytes proliferation of fibroblasts, endothelial, and other cells;
stimulates ECM protein synthesis

Fibroblast growth Macrophages, mast cells, Chemotactic and mitogenic for fibroblasts; stimulates
factors (FGFs), endothelial cells, many other angiogenesis and ECM protein synthesis
cell types
Including acidic (FGF-
1) and basic (FGF-2)

Transforming growth Platelets, T lymphocytes, Chemotactic for leukocytes and fibroblasts; stimulates
factor-β (TGF-β) macrophages, endothelial ECM protein synthesis; suppresses acute Inflammation
cells, keratinocytes, smooth
muscle cells, fibroblasts

Keratinocyte growth fibroblasts Stimulates keratinocyte migration, proliferation, and

factor (KGF) (i.e., differentiation
FGF-7)

ECM Extracellular membrane.

16. A, B, C, E
Pluripotency of embryonic stem cell depends on expression of following transcription
factors-
1. Oct 3/4
2. Sox 2
3. C-Myc
4. Kfl 4
5. ckit
Pluripotency of embryonic stem cell is inhibited by home box protein ‘Nanog’.

17. B
The two most common forms of DNA variation in the human genome are single-
nucleotide polymorphisms (SNPs) and copy number variations (CNVs). SNPs are
variants at single nucleotide positions and are almost always biallelic (i.e., only two
choices exist at a given site within the population, such as A or T). Much effort has
been devoted to mapping common SNPs in human populations. Over 6 million human
SNPs have been identified, many of which show wide variation in frequency in
different populations. SNPs occur across the genome—within exons, introns, intergenic
regions, and coding regions. Overall, about 1% of SNPs occur in coding regions, which
is about what would be expected by chance, since coding regions comprise about
1.5% of the genome. SNPs located in non-coding regions may fall in regulatory
elements in the genome, thereby altering gene expression; in such instances the SNP
may have a direct influence on disease susceptibility. In other instances, the SNP may
be a “neutral” variant that has no effect on gene function or carrier phenotype.
However, even “neutral” SNPs may be useful markers if they happen to be co-inherited
with a disease-associated gene as a result of physical proximity. In other words, the
SNP and the causative genetic factor are in linkage disequilibrium. There is hope that
groups of SNPs may serve as markers of risk for multigenic complex diseases such as
type II diabetes and hypertension. However, the effect of most SNPs on disease
susceptibility is weak, and it remains to be seen if identification of such variants, alone
or in combination, can be used to develop effective strategies for disease prevention

18. A
Laminin is the most abundant glycoprotein. Lamin is an intermediate filament of the
cytosol.
Fibronectin is a component of the extra cellular matrix, not cytoplasm.
 FACITs (fibril-associated collagen with interrupted triple helices), such as type IX
collagen are in cartilage.

19. C

20. A

Tissue and Stem Cells Location Extra

Bone marrow= HSCs HSCs can be collected from bone marrow, Bone marrow produces 1.5 x
and MSCs umbilical cord blood and peripheral blood of 106 blood cells per second
individuals receiving CSF’s

Liver- Oval cells Canal of Hering- junction between the biliary ductal Activated only when hepatocyte
(Bipotential- system and parenchymal hepatocytes proliferation is stopped
hepatocytes or biliary
cells)

Brain- Neural Stem Cells Subventricular zone and Dentate gyrus of Capable of generating neurons,
(NSCs) Hippocampus astrocytes and
oligodendrocytes

Skin Hair Follicle Bulge Activated by Wnt pathway and

inhibition of signalling from BMP
Interfollicular area of surface epidermis pathway

Sebaceous glands

Intestine Above paneth cells in SI and base of crypt in case Wnt and BMP pathways
of colon

Skeletal Muscle Beneath myocyte basal lamina Regeneration is through

Satellite cell replication

Cornea At the junction between the epithelium of cornea Limbal Stem Cells (LSCs)
and conjunctiva

21. B
22. A

23. c
 Cell Adaptation, Injury and Death –
Questions
24. True about Metaplasia is?
a. Involves only epithelial cells
b. Is irreversible
c. Can occurs at stem cells level
d. Columnar is the most common type

25. All of the following true regarding hypertrophy except:

a. Increased in cell size without increase in number
b. DNA content same as in normal cells
c. Increase in cell size is due to synthesize of more cellular proteins
d. Associated with a switch of contractile proteins from adult to fetal or neonatal
forms

26. Find the false statement about metaplasia:

a. Reversible
b. No loss of polarity
c. Reprogramming of stem cells
d. Pleomorphism present

27. Increase in the number of goblet cells in the non-respiratory terminal

bronchiole is an example of:
a. Anaplasia
b. Dysplasia
c. Metaplasia
d. Hyperplasia

28. In respiratory tract metaplasia occurs from:

a. Squamous to columnar
b. Columnar to cuboidal
c. Columnar to squamous
d. Cuboidal to squamous

29. In Vitamin-A deficiency, cancerous lesions occur due to-

a. Metaplasia
b. Dysplasia
c. Aplasia
d. Hyperplasia

30. All are cellular adaptations except:

a. Hypertrophy
b. Hyperplasia
 c. Necrosis
d. Metaplasia

31. Features of irreversible cell injury is/are? (PGI type)

a. Lysosomal rupture
b. Pyknosis
c. Bleb formation on membrane
d. Severe mitochondrial dysfunction

32. In myocardium reperfusion injury is due to?

a. Ca
b. Mg
c. K
d. Mn

33. Which of the following is not a sign of reversible cell injury?

a. ATP depletion
b. Cell shrinkage
c. Fatty acid deposition
d. Reduction of phosphorylation

34. Cells seen in chronic infection of pseudomonas:

a. Neutrophils
b. Eosinophils
c. Lymphocytes
d. Macrophage

35. For programmed cell death and autopagy, which is pro apoptotic genes?
a. BCL2
b. BAX
c. BCL-XL
d. BIM
24. c 25. b 26. d 27. c 28. c 29. a 30. c 31. 32. a 33. b 34. a
a,d

35. b

36. True about p53 gene? (PGI type)

a. Tumor suppression
b. Proapoptotic
c. Antiapoptotic
d. Cell repair
e. Oncogene

37. True about caspases are?

a. They are enzymes starting apoptosis
 b. They inhibit apoptosis
c. They are receptors of apoptosis
d. They are proteases which cause cellular death in apoptosis

38. True about necroptosis is all except?

a. Caspase 1 & 11 is involved
b. Caspase independent
c. Failure of activation of caspase 8
d. Lipid peroxidation is seen

39. SMAC/DIAMBLO is a:
a. Anti apoptotic protein
b. Induces necrosis
c. Acts both as anti and pro apoptotic protein
d. Pro-apoptotic protein

40. Which of the following is an execution caspase:

a. Caspase 3
b. Caspase 5
c. Caspase 8
d. Caspase 9

41. Annexin V is a marker of-

a. Necrosis
b. Gangrene
c. Aging
d. Apoptosis

42. The following is not a sensor of apoptosis:

a. Puma
b. Noxa
c. BAX
d. BAD

43. Intrinsic pathway of apoptosis is initiated by all the following except:

a. Growth factor withdrawal
b. DNA damage
c. Protein misfolding
d. Type 1 TNF receptor

44. Defective apoptosis and increased cell survival is seen in:

a. Autoimmune disease
b. Neurodegenerative diseases
c. Viral infections
d. Ischemic injury
45. Receptor associated kinases 1 (RIP1) and 3 (RIP3) are involved in:
a. Necrosis
b. Apoptosis
c. Necroptosis
d. Pyroptosis

46. Inflammasome is formed in:

a. Necrosis
b. Apoptosis
c. Necroptosis
d. Pyroptosis

47. Fibrinoid necrosis is seen in all of the following except:

a. Malignant hypertension
b. Aschoff’s nodule
c. Polyarteritis nodosa
d. Diabetic glomerulosclerosis

48. Dystrophic calcification is/are found in? (PGI type)

a. Monckeberg’s medical sclerosis
b. Papillary carcinoma thyroid
c. Hyperparathyroidism
d. Meningioma
e. Vitamin D intoxication

49. Highest telomerase activity is seen in:

a. Stem cells
b. Somatic cells
c. Germ cells
d. Benign tumors

50. Organelle where H2O2 is produced and destroyed is:

a. Peroxisome
b. Lysosome
c. Golgi body
d. Ribosome

51. Which of these is not responsible for removal of free radicals?

a. Catalase
b. Superoxide Dismutase
c. NADPH oxidase
d. Glutathione peroxidase
36. 37. d 38. a 39. d 40. a 41. d 42. c 43. d 44. a 45. c 46. d
a, b,
d
47. d 48. 49. c 50. a 51. c
a, b,
d

52. Endometrial adenocarcinoma is caused by

a. Hyperplasia
b. Atrophy
c. Both
d. None

53. Metaplasia of respiratory tract is due to

a. Vitamin E deficiency
b. Vitamin K deficiency
c. Vitamin A deficiency
d. Vitamin D deficiency

54. In cell death, myelin figures are derived from-

a. Nucleus
b. Cell membrane
c. Cytoplasm
d. Mitochondria

55. The sign of reversible injury in a case of alcoholic liver disease-

a. Loss of cell membrane
b. Nuclear karyolysis
c. Cytoplasmic vacuole
d. Pyknosis

56. Irreversible cell injury is indicated by-

a. Accumulation of calcium in mitochondria
b. Myelin figures
c. ATP depletion
d. Shifting of ribosomes

57. Type of necrosis occurring in brain-

a. Coagulative
b. Liquefactive
c. Fibrinoid
d. Caseous

58. Fat necrosis is common in-

a. Omentum
b. Breast
c. Retroperitoneal fat
d. All of the above
59. Example of apoptosis is-
a. Councilman bodies
b. Gamma gandy body
c. Russell bodies
d. None

60. Characteristic feature of apoptosis-

a. Cell membrane intact
b. Cytoplasmic eosinophilia
c. Nuclear moulding
d. Cell swelling

61. A 55-years-old male who has a long history of excessive drinking presents
with signs of alcoholic hepatitis. Microscopic Examination of a biopsy of this
patient’s liver reveals irregular eosinophilic hyaline inclusions within the
cytoplasm of the hepatocytes. These eosinophilic inclusions are composed
of:
a. Immunoglobulin
b. Excess plasma proteins
c. Keratin intermediate filaments
d. Lipofuscin

62. Characteristic feature of apoptosis-(PGI)

a. Cell membrane intact
b. Cytoplasmic eosinophilia
c. Nuclear moulding
d. Cell Shrinkage

63. Lipofuscin granules are examples of

a. Apoptotic bodies
b. Residual bodies
c. Psammomatous calcification
d. Hyaline change

64. Squamous metaplasia is seen in all of the following except

a. Vitamin A deficiency
b. Smoking
c. Gastroesophageal reflux disease
d. Stone obstructing a duct

65. All of the following are true about apoptosis except

a. Cell shrinkage
b. Altered orientation of lipids
c. Only pathological
d. No adjacent inflammation

66. All are true about reversible cell injury except

 a. Cellular swelling is the earliest manifestation
b. Organ shows increased turgor and has decreased weight
c. Clear vacuoles represent distended and pinched off ER
d. Increased eosinophilia of cytoplasm
52. c 53. c 54. b 55. c 56. a 57. b 58. d 59. a 60. a 61. c 62.
a, d

63. b 64. c 65. c 66. b

67. Which of the following is/are true about the microscopic appearance of
necrotic cells?
a. Increased eosinophilia due to loss of cytoplasmic RNA
b. Increased eosinophilia due to denaturation of cytoplasmic proteins
c. Glassy homogenous appearance due to loss of glycogen particles
d. All of the above

68. Which phenomenon/phenomena characterise irreversibility of cell injury?

a. Mitochondrial dysfunction
b. Profound membrane damage
c. Nuclear disaggregation
d. Both A and B

69. All of the following are pro apoptotic except

a. Smac
b. Diablo
c. BAX
d. BCL- XL

70. All of the following is/are true about extrinsic pathway of apoptosis except
a. Engagement of plasma membrane death receptors
b. Type I TNF receptor is prototype
c. Caspase 9 is classically involved
d. Mechanism of apoptosis of virus infected cells

71. Programmed necrosis is another name for

a. Necroptosis
b. Pyroptosis
c. Atrophy
d. Autophagy

72. Macrophage-specific deletion of which autophagy related gene increases

susceptibility to tuberculosis
a. Atg 3
b. Atg 4
c. Atg 5
d. Atg 6
73. Which of the following is false about lipofuscin?
a. Injurious to cell
b. Perinuclear in location
c. Lipid peroxidation
d. Yellow brown granular pigment

74. All are examples of metastatic calcification except

a. Milk Alkali syndrome
b. Hyperparathyroidism
c. Renal osteodystrophy
d. Atherosclerosis

75. Metaplasia arises from reprograming of-

a. Stem cells
b. Stellate cells
c. Squamous cells
d. Columnar cells

76. “Caspase-independent” programmed cell death-

a. Necrosis
b. Necroptosis
c. Apoptosis
d. None

77. Immune complexes mediated necrosis is of which type?

a. Coagulative necrosis
b. Liquefactive necrosis
c. Caseous necrosis
d. Fibrinoid necrosis

78. Stain for fat all except:

a. Oil red O
b. Sudan black
c. Sudan III
d. Congo red

79. The enzyme that protects brain from free radical injury:
a. Superoxide dismutase
b. Catalase
c. Glutathione peroxidase
d. Monoamine oxidase

80. Physiological hyperplasia and hyper-trophy are seen simultaneously in-

a. Uterus in pregnancy
b. Skeletal muscle in athletes
c. Breast at puberty
 d. Thyroid gland during pregnancy

81. All are reversible injury of cell, except-

a. Vacuole
b. Karyorrhexis
c. Fat accumulation
d. Cell wall swelling

67. d 68. d 69. d 70. c 71. a 72. c 73. a 74. d 75. a 76. b 77. d

78. d 79. a 80. 81. b

a,c

82. Fibrinoid necrosis is seen in following except-

a. Pan
b. Diabetes mellitus
c. Malignant hypertension
d. SLE

83. Esoinophilia in necrosed tissue is due to

a. Coagulation of proteins
b. Denaturation of enzymes
c. Lysosomal damage
d. Mitochondrial damage

84. True about apoptosis are all except-

a. Inflammation is present
b. Chromosomal breakage
c. Clumping of chromatin
d. Cell shrinkage

85. CD-95 is a marker of-

a. Death receptor
b. MHC complex
c. T helper cells
d. NK cells

86. True about apoptosis is-

a. Energy dependent
b. Self-initiated
c. Swelling of cytoplasm
d. Loss of membrane integrity

87. CD-95 has a major role in-

a. Apoptosis
b. Cell necrosis
c. Interferon activation
 d. Proteolysis

88. Which of the following organelles plays a pivotal role in apoptosis?

a. Mitochondria
b. Endoplasmic reticulum
c. Nucleus
d. Golgi apparatus

89. Cytosolic cytochrome C plays an important function in-

a. Apoptosis
b. Cell necrosis
c. Electron transport chain
d. Cell division

90. CD-95 is a marker of-

a. Intrinsic pathway of apoptosis
b. Extrinsic pathway of apoptosis
c. Monocyte
d. Leucocyte

91. In apoptosis, cytochrome C acts through-

a. Apaf-1
b. BCL-2
c. FADD
d. TNF

92. Which of the following has a direct role in apoptosis-

a. Nitric oxide
b. Adenyl cyclase
c. cAMP
d. Cytochrome C

93. The following is a antiapoptotic gene-

a. Bax
b. Bad
c. BCL-XL
d. Bim

94. SMAC/DIABLO
a. Anti-Apoptotic proteins
b. Induces necrosis most often
c. It can act as both apoptotic and antiapoptotic proteins
d. Pro-apoptotic proteins

95. Which of the following is an antiapoptotic gene?

a. C-myc
 b. P53
c. BCL-2
d. Bax

96. Brown atrophy is due to accumulation of-

a. Melanin
b. Hemosiderin
c. Hematin
d. Lipofuscin

97. Which of the following pigments are involved in free radical injury?
a. Lipofuscin
b. Melanin
c. Bilirubin
d. Hematin

98. Dystrophic calcification is seen in-

a. Milk alkali syndrome
b. Atheromatous plaque
c. Hyperparathyroidism
d. Vitamin A intoxication
82. b 83. a 84. a 85. a 86. a 87. a 88. a 89. a 90. b 91. a 92. d

93. c 94. d 95. c 96. d 97. a 98. b

99. True about psammoma bodies are all except-

a. Seen in meningioma
b. Concentric whorled appearance
c. Contains calcium deposits
d. Seen in teratoma

100. Calcification of soft tissues without any disturbance of calcium

metabolism is called-
a. Ionotrophic calcification
b. Monotrophic calcification
c. Dystrophic calcification
d. Calcium induced calcification

101. Metastatic calcification is not seen in-

a. Kidney tubules
b. Fundal glands of stomach
c. Alveoli of lungs
d. Media of Monckeberg degeneration

102. Apoptosis is inhibited by-

a. P53
 b. N-myc
c. RAS
d. BCL-2

103. Calcification in necrotic tissue is called-

a. Metastatic calcification
b. Dystrophic calcification
c. Calcinosis
d. Tumoral calcinosis

104. Increase in this patient’s serum enzyme (e.g. AST/ALT) Levels are seen in
hepatitis. Most likely this results from?
a. Autophagy by lysosomes
b. Clumping of nuclear chromatin
c. Defects in the cell membrane
d. Swelling of the mitochondria

105. Which of the following cells is most likely to have the highest telomerase
activity?
a. Endothelial cells
b. Germ cells
c. Neutrophils
d. Erythrocytes

106. Hypertrophy is a type of –

a. Cell injury
b. Cellular adaptation
c. Carcinoma
d. Cell aging

107. Which finding on electron microscopy indicates irreversible cell injury -

a. Dilatation of endoplasmic reticulum
b. Dissociation of ribosomes from rough endoplasmic reticulum
c. Flocculent amorphous densities in the mitochondria
d. Myelin figures

108. Irreversible cell injury is indicated by-

a. Accumulation of calcium in cytosol
b. Myelin figures
c. ATP depletion
d. Shifting of ribosomes

109. In cell death, myelin figures are derived from -

a. Nucleus
b. Cell membrane
c. Cytoplasm
 d. Mitochondria

110. MI is a type of-

a. Coagulative necrosis
b. Liquefactive necrosis
c. Caseous necrosis
d. Fat necrosis
99. d 100. c 101. 102. 103. 104. c 105. 106. b 107. 108. a
d d b b c,d

109. 110.
b a
 Cell Adaptation, Injury and Death –
Explanations
24. C
Metaplasia is a change in phenotype of differentiated cells, often in response to
chronic irritation, that makes cells better able to withstand the stress; usually
induced by altered differentiation pathway of tissue stem cells; may result in
reduced functions or increased propensity for malignant transformation.
Option A- Both epithelial and mesenchymal metaplasia can be seen
Option B- it is a reversible adaptation
Option D- Squamous metaplasia is the most common type

25. B
Cell size is increased by increase in protein synthesis hence genes unexpressed or
silent before are now expressed which leads to an increase in DNA content.
Other statements are true.

26. D
Pleomorphism is a feature of dysplasia and anaplasia, so is loss of polarity.
Other options are true.
Refer to the answer above for more details.

27. C
Change in cell type is metaplasia.
Option A- histological hallmark of malignancy
Option B- disordered growth
Option D- increase in number of cells (not change in cells)

28. C
The normal pseudostratified ciliated columnar epithelium of respiratory tract is
replaced by stratified squamous epithelium in response to smoking.
Option A- Barret’s esophagus (intestinal metaplasia)

29. A
Squamous metaplasia is a common consequence of vitamin A deficiency. (Lung
cancer has been recently implicated with this mechanism)

30. C
Option A-Increase in cell size
Option B-Increase in cell number
Option C- Cell death
Option D- change in cell type

31. A, D
Reversible to irreversible cell injury is a spectrum and can show similar features.
Some however are more indicative of irreversible cell injury.
32. A
Reference : Robbins and Cotran Pathological Basis of Disease, 9th edition
The factors that contribute to reperfusion injury in the myocardium include the
following:
Mitochondrial dysfunction: Mitochondrial permeability increases → apoptosis
activated
Myocyte hypercontracture due to increased levels of intracellular calcium → After
reperfusion, the contraction of myofibrils is augmented and uncontrolled, causing
cytoskeletal damage and cell death.
Free radicals, including superoxide anion (•O2 − ), hydrogen peroxide (H2O2),
hypochlorous acid (HOCl), nitric oxide–derived peroxynitrite, and hydroxyl radicals
(•OH)
Leukocyte aggregation may occlude the microvasculature and contribute to the “no-
reflow” phenomenon. Further, leukocytes elaborate proteases and elastases that
cause cell death.
Platelet and complement activation also contribute to microvascular injury.
Complement activation is thought to play a role in the no-reflow phenomenon by
injuring the endothelium.

33. B
Option A- ATP depletion is one of the earliest biochemical changes occurring in cell
injury
Option B- Feature of apoptosis (cell death, not reversible cell injury)
 Option C- Cellular swelling and fatty change are earliest findings of reversible cell
injury
Option D- Depletion of ATP is a consequence of reduced phosphorylation

34. A
Option A- Although cells of acute inflammation, in some infections they persist even
when chronic infection continues like in Pseuodomonas
Option B- Seen in parasitic infections and allergic reactions
Option C- Seen in chronic inflammation and viral infections
Option D- Seen in chronic inflammation

35. B
Option .12 A and C are anti apoptotic
Option B- pro apoptotic
Option D- sensor protein

36. A, B, D
Options C and E are not the function of p53 which serves as a guardian of the genome.

37. D
Best option here is option D. Caspases are not the first enzymes activated in apoptosis
but they are cysteine proteases involved in protein breakdown leading to apoptosis

38. A
Option A- feature of pyroptosis
Option B- caspase independent programmed cell death
Option C- after death receptor interaction failure to activate caspase 8 can lead to
activation of necroptosis
Option D- free radical damage is a part of the mechanism of cell death by necroptosis

39. D
Smac and Diablo are released from the mitochondria when there is increased
mitochondrial permeability and they inactivate Inhibitors of Apoptosis (IAPs) which
inactivate caspases, thus letting caspases function and promoting apoptosis.

40. A
Caspase 3, 6 and 7 are execution caspases
Caspase 8 is an initiator caspase of extrinsic pathway
Caspase 9 is an initiator caspase of intrinsic pathway

41. D
TUNEL is an acronym for terminal deoxynucleotidyl transferase biotin-dUTP nick end
labeling. Terminal deoxynucleotidyl transferase (TdT) is a template-independent DNA
polymerase that is normally active in primitive lymphoid cells to increase receptor
diversity.
TdT can add random nucleotides to the ends of DNA fragments produced by
endonucleases during apoptosis, since 3′ phosphate groups are the substrate for TdT
(3′ phosphate groups are not produced during cell necrosis). Treating tissue sections
with TdT and labeled nucleotides then provides a convenient assay for apoptosis. In
 practice, necrotic debris may nonspecifically trap either fluorescent or chromogenic
signals and result in a false-positive assay. Apoptosis can also be detected by means of
assays for activated caspase-3, Fas ligand, and annexin V.

42. C
Option C- Pro apoptotic
Options A, B, D- Sensor of apoptosis

43. D
Option A, B, C- intrinsic pathway
Option D- death receptor or extrinsic pathway

44. A
Defective apoptosis and increased cell survival of cells which should have died is seen
in autoimmune disease and cancer.
Increased apoptosis and decreased cell survival of cells which should not have died is
seen in the other three options.

45. C
Interaction of TNFR and inactivation of caspase 8 leads to activation of RIP1 and RIP3
to cause necroptosis
Option A- lysosomal enzymes
Option C- Caspases 3, 6, 8, 9, 10
Option D- Caspases 1 and 11

46. D
Microbial products that enter the cytoplasm of infected cells are recognized by
cytoplasmic innate immune receptors and can activate the multiprotein complex
called the inflammasome. The function of the inflammasome is to activate caspase1,
(also known as interleukin-1β converting enzyme) which cleaves a precursor form of
IL-1 and releases its biologically active form. IL-1 is a mediator of many aspects of
inflammation, including leukocyte recruitment and fever. Caspase-1 and, more
importantly, the closely related caspase-11 also induce death of the cells. Unlike
classical apoptosis, this pathway of cell death is characterized by swelling of cells, loss
of plasma membrane integrity, and release of inflammatory mediators. Pyroptosis
results in the death of some microbes that gain access to the cytosol and promotes the
release of inflammasome-generated IL-1.

47. D
Fibrinoid necrosis is a special form of necrosis usually seen in immune reactions
involving blood vessels. This pattern of necrosis typically occurs when complexes of
antigens and antibodies are deposited in the walls of arteries. Deposits of these
“immune complexes,” together with fibrin that has leaked out of vessels, result in a
bright pink and amorphous appearance in H&E stains, called “fibrinoid” (fibrin-like) by
pathologists. This pattern of necrosis is seen classically in options A, B and C as well as
rejection of transplants.

48. A, B, D
Dystrophic calcification seen in dying tissues with normal calcium levels.
 Option C and E are examples of metastatic calcification seen in normal tissues with
increased calcium levels.

49. C
Telomere length is maintained by nucleotide addition mediated by an enzyme called
telomerase. Telomerase is a specialized RNA-protein complex that uses its own RNA as
a template for adding nucleotides to the ends of chromosomes. Telomerase activity is
expressed in germ cells and is present at low levels in stem cells, but it is absent in
most somatic tissues

50 A

Properties O2 H2 O2 *Oh

Mechanisms Incomplete reduction of O2 during Generated by SOD from Generated from H2O by
of oxidative phosphorylation; by O2 and by oxidases in hydrolysis, e.g., by
production phagocyte oxidase in leukocytes peroxisomes radiation; from H2 O2 by
Fenton reaction; from O2

Mechanisms Conversion to H2 O2 and O2 by Sod Conversion to H2 O and O2 Conversion to H2 O by

of by catalase (peroxisomes), glutathione peroxidase
inactivation glutathione peroxidase
(cytosol, mitochondria)

Pathologic Stimulates production of degradative Can be converted to *OH Most reactive oxygen-
effects enzymes in leukocytes and other cells; and OCI_ , which destroy derived free radical;
may directly damage lipids, proteins, microbes and cells; can act principal ROS responsible
DNA; acts close to site of production distant from site of for damaging lipids,
production proteins, and DNA

51. C
helps to generate free radicals especially in neutrophils

52. C
Type I endometrial adenocarcinoma arises in a hyperplastic endometrium whereas
Type II may arise in an atrophic endometrium

53. C
In the habitual cigarette smoker, the normal ciliated columnar epithelial cells of the
trachea and bronchi are often replaced by stratified squamous epithelial cells. Stones
in the excretory ducts of the salivary glands, pancreas, or bile ducts, which are
normally lined by secretory columnar epithelium, may also lead to squamous
metaplasia by stratified squamous epithelium. A deficiency of vitamin A (retinoic acid)
induces squamous metaplasia in the respiratory epithelium.

54. B
Phospholipids derived myelin figures are more characteristic for irreversible than
reversible cell injury.

55. C
Cellular swelling and organelle swelling are signs of reversible cell injury

56. A
Influx of calcium into mitochondria increases its permeability thus causing a cascade
of changes responsible for cellular death.
57. B
Enzymatic digestion by both enzymes released from dying cells and inflammatory
cells causes lysis of the dead cells into a liquefied viscous mass- liquefactive necrosis.
Option A- Most common pattern of ischemic necrosis in all organs other than brain
Option C- Usually in vasculitis
Option D- Central necrosis leading to cheese like necrosis on gross

58. D
All sites are fat rich and hence digestion of fatty cells and their membranes followed
by saponification into calcium salts is relatively common in these sites.

59. A
Option B- Calcified bodies seen in congestive splenomegaly
Option C- Intracellular accumulation of Igs in plasma cells

60. A
Intact cell membrane and no inflammation is characteristic of apoptosis. Other
features are more classical for necrosis.

61. C
CK 8/18- Mallory hyaline

62. A, D
Option B- feature of necrosis more than apoptosis

63. B
Autophagy (“self-eating”) is the process in which the starved cell eats its own
components in an attempt to reduce nutrient demand to match the supply. Some of
the cell debris within the autophagic vacuoles may resist digestion and persist in the
cytoplasm as membrane-bound residual bodies. An example of residual bodies is
lipofuscin granules.

64. C
Options A, B, D are examples of change of columnar epithelium to squamous. However
GERD in esophagus causes change of squamous to columnar (called Intestinal
Metaplasia or Barret’s Esophagus)

65. C

Feature Necrosis Apoptosis

Cell size Enlarged (swelling) Reduced (shrinkage)

Nucleus Pyknosis → karyorrhexis → Fragmentation into nucleosome size fragments & condensation
karyolysis of chromatin

Plasma Disrupted Intact; altered structure, especially orientation of lipids

membrane

Cellular Enzymatic digestion; may Intact; may be released in apoptotic bodies

contents leak out of cell
Adjacent Frequent No
inflammation

Physiologic or Invariably pathologic Often physiologic, means of eliminating unwanted cells; may be
pathologic (culmination of irreversible pathologic after some forms of cell injury, especially DNA damage
role cell injury)

66. B
Cellular swelling is the first manifestation of almost all forms of injury to cells.
It is a difficult morphologic change to appreciate with the light microscope; it may be
more apparent at the level of the whole organ.
When it affects many cells, it causes some pallor, increased turgor, and increase in
weight of the organ.
On microscopic examination, small clear vacuoles may be seen within the cytoplasm;
these represent distended and pinched-off segments of the ER → Hydropic change or
vacuolar degeneration.
Swelling of cells is reversible.
Cells may also show increased eosinophilic staining, which becomes much more
pronounced with progression to necrosis

67. D
Necrotic cells show increased eosinophilia in hematoxylin and eosin (H & E) stains,
attributable in part to the loss of cytoplasmic RNA (which binds the blue dye,
hematoxylin) and in part to denatured cytoplasmic proteins (which bind the red dye,
eosin). The necrotic cell may have a more glassy homogeneous appearance than do
normal cells, mainly as a result of the loss of glycogen particles. When enzymes have
digested the cytoplasmic organelles, the cytoplasm becomes vacuolated and appears
moth-eaten.

68. D
Two phenomena consistently characterize irreversibility—the inability to reverse
mitochondrial dysfunction (lack of oxidative phosphorylation and ATP generation) even
after resolution of the original injury, and profound disturbances in membrane
function. Injury to lysosomal membranes results in the enzymatic dissolution of the
injured cell that is characteristic of necrosis.

69. D
Smac/Diablo, enter the cytoplasm, where they bind to and neutralize cytoplasmic
proteins that function as physiologic inhibitors of apoptosis (called IAPs).
The normal function of the IAPs is to block the activation of caspases, including
executioners like caspase-3, and keep cells alive. Thus, the neutralization of these
IAPs permits the initiation of a caspase cascade.
BAX and BAK are the two prototypic members of the BCL2 family.
BCL XL, MCL1 and BCL2 are the anti apoptotic members

70. C
Caspase 8 and 10 (in humans) are involved in the extrinsic pathway

71. A
The following features characterize necroptosis:
 Morphologically, and to some extent biochemically, it resembles necrosis, both
characterized by loss of ATP, swelling of the cell and organelles, generation of ROS,
release of lysosomal enzymes and ultimately rupture of the plasma membrane as
discussed earlier.
Mechanistically, it is triggered by genetically programmed signal transduction events
that culminate in cell death. In this respect it resembles programmed cell death,
which is considered the hallmark of apoptosis
Because of the duality of these features, necroptosis is sometimes called programmed
necrosis to distinguish it from the more usual forms of necrosis driven passively by
toxic or anoxic injury to the cell.
In sharp contrast to apoptosis, the genetic program that drives necroptosis does not
result in caspase activation and hence it is also sometimes referred to as “caspase-
independent” programmed cell death.

72. C
Many pathogens are degraded by autophagy; these include mycobacteria, Shigella
spp., and HSV-1. This is one way by which microbial proteins are digested and
delivered to antigen presentation pathways. Macrophage-specific deletion of Atg5
increases susceptibility to tuberculosis.

73. A
Lipofuscin is not injurious to the cell or its functions. Its importance lies in its being a
telltale sign of free radical injury and lipid peroxidation. The term is derived from the
Latin ( fuscus, brown), referring to brown lipid. In tissue sections it appears as a
yellow-brown, finely granular cytoplasmic, often perinuclear, pigment.

74. D
There are four principal causes of hypercalcemia:
(1) increased secretion of parathyroid hormone (PTH) with subsequent bone
resorption, as in hyperparathyroidism due to parathyroid tumors, and ectopic secretion
of PTH-related protein by malignant tumors;
(2) resorption of bone tissue, secondary to primary tumors of bone marrow (e.g.,
multiple myeloma, leukemia) or diffuse skeletal metastasis (e.g., breast cancer),
accelerated bone turnover (e.g., Paget disease), or immobilization;
(3) vitamin D–related disorders, including vitamin D intoxication, sarcoidosis (in which
macrophages activate a vitamin D precursor), and idiopathic hypercalcemia of infancy
(Williams syndrome), characterized by abnormal sensitivity to vitamin D; and
(4) renal failure, which causes retention of phosphate, leading to secondary
hyperparathyroidism.
Less common causes include aluminum intoxication, which occurs in patients on
chronic renal dialysis, and milk-alkali syndrome, which is due to excessive ingestion of
calcium and absorbable antacids such as milk or calcium carbonate

75. A
Refer to answer above for details.

76. B
Refer to explanation above

77. D
 Refer to explanation above

78. D
Option D is a stain used for Amyloid

79. A (single best answer)

80. A, C

81. B
Refer to the explanation provided before

82. B
Refer to the explanation provided above

83. A
Refer to the explanation provided above

84. A
Refer to the explanation provided above

85. A
Refer to the explanation provided above

86. A

87. A
Refer to the explanation provided above

88. A
Refer to the explanation provided above

89. A
Refer to the explanation provided above

90. B
Refer to the explanation provided above

91. A
Refer to the explanation provided above

92. D

93. C

94. D

95. C

96. D

97. A
Another Random Scribd Document
with Unrelated Content
considerable sums of money. For his part, he said, he had nothing; if
in the course of time, he should find himself in possession of any
property in Europe, he should be wholly indebted for it to the
foresight and contrivance of some of his friends.
If the Emperor had gone to America, he intended to have collected
all his relatives around him; and he supposed that they might have
realized at least forty millions of francs. This point would have
become the nucleus of a national union, a second France. Before the
conclusion of a year, the events of Europe would have collected
around him a hundred millions of francs and sixty thousand
individuals, most of them possessing wealth, talent, and information.
The Emperor said that he should have liked to realize that dream; it
would have been a renewal of his glory.
“America,” continued he, “was in all respects our proper asylum. It is
an immense continent, possessing the advantages of a peculiar
system of freedom. If a man is troubled with melancholy, he may get
into a coach, and drive a thousand leagues, enjoying all the way the
pleasure of a common traveller. In America you may be on a footing
of equality with every one; you may, if you please, mingle with the
crowd, without inconvenience, retaining your own manners, your
own language, your own religion, &c.”
He said it was impossible that he could henceforth consider himself
as a private man in Europe; his name was too popular throughout
the continent. He was in some way or other connected with every
people, and belonged to every country.
“As for you,” said he to me smiling, “your fate seemed naturally to
lead you to the shores of the Oronooko or to Mexico, where the
recollection of the good Las Cases is not yet obliterated. You would
there have enjoyed all you could have wished. The destinies of some
men seem to be marked out. Gregoire, for instance, has only to go
to Hayti, and he would immediately be made a Pope.”
At the time of the Emperor’s second abdication, an American in Paris
wrote to him as follows:—"While you were at the head of a nation,
you could perform any miracle, you might conceive any hopes; but
now you can do nothing more in Europe. Fly to the United States! I
know the hearts of the leading men and the sentiments of the
people of America. You will there find a second country and every
source of consolation." The Emperor would not listen to such a
suggestion. He might, doubtless, by dint of speed or disguise, have
gained Brest, Nantes, Bordeaux, or Toulon, and in all probability
have reached America; but he conceived that either disguise or flight
would be derogatory from his dignity. He thought himself bound to
prove to all Europe his full confidence in the French people, and their
extreme attachment to him, by passing through his dominions at
such a crisis, merely in the quality of a private man, and unattended
by any escort. But what above all influenced him at that critical
moment was the hope that impending dangers would open the eyes
of his subjects, that they would rally around him, and that he might
save the country. This hope caused him to linger at Malmaison, and
to postpone his departure, after he had reached Rochefort. If he is
now at St. Helena, he owes his captivity to this sentiment, of which
he was unable to divest himself. Subsequently, when he had no
other resource than to accept the hospitality of the Bellerophon, it
was not perhaps without a feeling of inward satisfaction that he
found himself, by the force of circumstances, irresistibly led to fix his
abode in England, where he might enjoy the happiness of being still
but little removed from France. He was well aware that he could not
be free in England; but he hoped to be heard, and then a chance
would at least have been open to the impressions which he might
create. “The English Ministers,” said he, “who are the enemies of
their country, and who have sold her to foreigners, thought they had
too much cause to dread my presence. They conceived that my
opinion in London would be more powerful than the whole
Opposition: that it would have compelled them either to change their
system or resign their places; and, to keep themselves in place, they
basely sacrificed the true interests of their country, the triumph, the
glory of her laws, the peace of the world, the welfare of Europe, the
happiness and the benedictions of posterity.”
In the course of conversation during the evening, the Emperor once
more adverted to Waterloo, and described his anxiety and indecision
before he came to a final resolution respecting his abdication. I pass
over a multitude of details, lest I should be led into repetition; I note
down only the following:—
The Emperor’s speech to his ministers was the literal prophecy of all
that subsequently took place. Carnot was the only one who seemed
to take a right view of the case. He opposed the abdication, which
he said was a death-blow to France; and he wished that we should
defend ourselves even to annihilation. Carnot was the only one who
maintained this opinion; all the rest were for the abdication. That
measure was determined, and Carnot, covering his face with his
hands, burst into tears.
At another moment the Emperor said, “I am not a God: I cannot do
all by my own single efforts: I cannot save the nation without the
help of the nation. I am certain that the people then entertained
these sentiments, and that they are now suffering undeservedly. It
was the host of intriguers, and men possessing titles and offices,
who were really guilty. That which misled them, and which ruined
me, was the mild system of 1814, the benignity of the restoration;
they looked for a repetition of this lenity. The change of the
Sovereign had become a mere joke. They all calculated on remaining
just as they had been before, whether I should be succeeded by
Louis XVIII. or any other. These stupid, selfish, and egotistical men
looked upon the great event as merely a competition, about which
they cared but little; and they thought only of their individual
interests, when a deadly war of principles was about to be
commenced. And why should I disguise the truth? There were
among the individuals whom I had elevated, and by whom I was
surrounded, a number of proud ...!” Then, turning to me, he added,
“I am not alluding to your Faubourg St. Germain, with respect to
which the matter was totally different, and for which some excuse
may be found. During my first reverses in 1814, the greatest traitors
were not the persons connected with that party, of whom I had no
great cause to complain; and, who, therefore, on my return, were
not bound to me by any particular ties of gratitude. I had abdicated,
the King was restored. They had but returned to their old
attachments, and had only renewed their allegiance.”

STATE OF FRENCH MANUFACTURES.—ON PHYSIOGNOMY.

27th.—The Emperor went out about 2 o’clock; the weather was very
fine. The season is sensibly different from that which we had on our
arrival; the air is infinitely more pure. The Emperor was, however,
very ill, and very low-spirited. He walked to the extremity of the
wood, while we were waiting for the calash. We took our usual drive.
The conversation turned on the state of manufactures in France. The
Emperor said he had raised them to a degree of prosperity hitherto
unknown; and which was scarcely credited in Europe, or even in
France. This was a subject of wonder to foreigners on their arrival.
The Abbé de Montesquiou, he said, was constantly expressing his
astonishment at this circumstance, the proofs of which he had in his
own hands, when he became Minister of the Interior.
The Emperor was the first individual in France who said: Agriculture,
first; industry, that is to say, manufactures, next; and, finally, trade,
which must arise out of the superabundance of the two first. He also
defined and put into practice, in a clear and connected way, the
systems most conducive to the interests of our manufacturers and
merchants. To him we were indebted for the cultivation of sugar,
indigo, and cotton. He offered a reward of a million francs to the
person who should discover a method of spinning flax like cotton;
and he doubted not that this discovery would have been made. The
fatality of circumstances alone prevented this grand idea from being
carried into execution.
“The old aristocracy, those enemies to our prosperity,” said the
Emperor, “exhausted all their wit in stupid jokes and frivolous
caricatures on these subjects. But the English had no cause to
laugh; they felt the blow, and have not yet recovered from it.”
A short time before dinner, the Emperor sent for me to attend him in
his chamber. He was very unwell; he tried to converse, but he had
not strength. He attributed his indisposition to his having drunk
some bad wine, which had newly arrived. He said that Corvisart,
Bertholet, and other physicians and chemists, had frequently said
that if he experienced the least unpleasant flavour, on first tasting
his wine, he must by no means swallow it.
The turn of the conversation led him to express his surprise at the
contrast between the character of the mind and the expression of
the countenance, which was observable in some individuals. “This
proves,” said he, "that we must not judge of a man by his face; we
can know him only by his conduct. What countenances have I had to
judge of in the course of my life! What odd samples of physiognomy
have come under my observation! And what rash opinions have I
heard on this subject! Thus I invariably made it a rule never to be
influenced either by features or by words. Still, however, it must be
confessed that we sometimes find curious resemblances between
the countenance and the character. For instance, on looking at the
face of our Monseigneur (meaning the Governor), who would not
recognise the features of a tiger-cat! I will mention another instance.
There was a man in my service, who was employed about my
person. I liked him very much; but I was obliged to dismiss him
because I several times caught him with his hands in my pockets. He
committed his thefts too impudently: let any one look at this man,
and they must admit that he has a magpie’s eye."
While we were conversing on the subject of physiognomy, some one
remarked, that Mirabeau, speaking of Pastoret’s face, said: “it is a
compound of the tiger and the calf; but the calf predominates.” At
this the Emperor laughed heartily, and said it was strictly true.
The Emperor wished to dine alone in his chamber. He sent for me
about ten o’clock. He was then better; and he looked over several of
the books which lay scattered upon his couch. He began to read
Racine’s Alexander, of which he expressed his dislike; and he
afterwards took up Andromache, which is one of his favourite pieces.
 MARKS OF RESPECT SHEWN TO THE EMPEROR BY THE
ENGLISH SOLDIERS.

28th.—The Emperor went out about two o’clock. The weather was
exceedingly pleasant. We took nearly an hour’s drive in the calash. It
had been at first proposed that the Emperor should ride on
horseback; for his health was suffering from the want of that
exercise. But he would not consent to go out on horseback; he said
that to ride backward and forward within the limits marked out for
him was like being confined in a riding-school, and he could not
endure it. However, on our return home, we succeeded in changing
his determination. We all attended him, and we reached the summit
of that part of Goat Hill which separates the horizon of the town
from that of Longwood. On our way back, we passed in front of the
English camp; this was the first time we had passed it since our
residence at Longwood. The soldiers immediately quitted their
various occupations, and eagerly formed themselves in a line as we
passed along. “What European soldier,” said the Emperor, “would not
be inspired with respect at my approach!” He knew this, and
therefore carefully avoided passing the English camp, lest he should
be accused of wishing to excite this sentiment. We all very much
enjoyed the ride, and returned home about five o’clock. The
Emperor was a little fatigued.
For some time past, he has relinquished his regular dictations. He
saw some skittles which had been made by the servants for their
own amusement. He ordered them to be brought to us, and we
played several games with them. The Emperor won a napoleon and
a half from me. He made me pay the debt, and then threw the
money to the servant who had attended us for the purpose of
running after the ball.

CORSICA.—REMARK MADE BY PAOLI.—MAGNANIMOUS CONDUCT OF MADAME

MÉRE.—LUCIEN INTENDED TO BE GOVERNOR-GENERAL OF CORSICA.—THE
FIRST CONSUL’S COURT.—MADAME DE CHEVREUSE.—THE EMPEROR
RECEIVES A LETTER FROM HIS MOTHER.
29th.—For some time past, at our urgent solicitation, the Emperor
every evening made a promise that he would ride on horseback
early on the following morning; but whenever the appointed hour
arrived he invariably changed his determination. This morning, he
was in the garden by half-past eight o’clock, and he sent for me. The
conversation turned on Corsica, and was maintained for upwards of
an hour.
"One’s native country," said he, “is always dear. Even St. Helena may
have charms to those who were born here.” To the Emperor,
therefore, Corsica presented a thousand attractions. He described
the grand scenery of the country, and remarked that islanders
always display originality of character, because their situation tends
to protect them against invasion, and precludes that perpetual
intercourse with foreigners which is experienced in continental
states. The inhabitants of mountainous regions, he said, always
possess a degree of energy, and a turn of mind peculiar to
themselves. He dwelt much on the charms of his native country,
which, from his early recollections, was to him superior to any other
spot in the world. He thought that the very smell of the earth would
enable him to distinguish his native land, even were he conducted
blindfold to her shores; there was in it something peculiar, which he
had never perceived elsewhere. Corsica was the scene of all his early
attachments; he had there passed the happy years of his childhood,
freely roaming among the hills and valleys, enjoying the honours
and pleasures of hospitality. He traced different lines of family
connections, who, he said, extended the spirit of animosity and
revenge, even to the seventh degree; and he observed that a young
woman in Corsica thought she enhanced the value of her dowry by
enumerating the list of her cousins. He recollected with pride that,
when only twenty years of age, he had accompanied Paoli on a
grand excursion to Porte di Nuovo. Paoli’s retinue was numerous; he
was escorted by upwards of 500 of his followers on horseback.
Napoleon rode by his side, and, as they went along, Paoli pointed
out to him the different positions and the places which had been the
scenes of resistance or triumph during the war for Corsican liberty.
He related to him all the particulars of that glorious conflict; and, on
hearing the remarks and opinions which fell from his young
companion, he said, "Oh Napoleon! there is nothing modern in your
character! you are formed entirely on Plutarch’s model."
When Paoli manifested his determination to surrender the island to
the English, the Bonaparte family continued to head the French
party, and had the fatal honour of being the object of a march of the
inhabitants of the island, that is to say, they were attacked by a levy
in mass: 12 or 15,000 peasants made a descent from the mountains
on Ajaccio. The house occupied by Napoleon’s family was pillaged
and burnt, and the vines and flocks were destroyed. Madame,
surrounded by a few faithful friends, wandered for some time on the
sea-shore, and was at length obliged to fly to France. The Bonaparte
family had always been much attached to Paoli, and he in his turn
had professed particular respect towards Madame. It is, however,
but just to remark that he employed persuasion before he resorted
to force. “Renounce this opposition,” said he, “it will prove the ruin
of yourself, your family, and your fortune; you will bring irreparable
misery on yourself.” The Emperor, indeed, affirmed that, but for the
chance of the revolution, the family could never have recovered from
their misfortunes. Madame, like another Cornelia, heroically replied,
“that she, her children, and her relatives would only obey two laws,
namely, those of duty and honour. Had old Archdeacon Lucien been
living at that time, his heart would have bled at the idea of the
danger of his sheep, goats, and cattle, and his prudence would not
have failed to allay the storm.”
Madame Bonaparte, the victim of her patriotism and her attachment
to France, expected to be received at Marseilles as an emigrant of
distinction; but there she scarcely found herself in safety; and, to
her astonishment, discovered that the spirit of patriotism existed
only among the very lowest classes of the people.
Napoleon, in his youth wrote a history of Corsica, which he
dedicated to the Abbé Raynal. This production gained for him some
flattering compliments and letters from the Abbé, who was the
fashionable author of the day. This history has been lost.
The Emperor remarked that, during the war in Corsica, all the
French who came to the island formed some decided opinion on the
character of the mountaineers. Some said that they were full of
enthusiasm, others regarded them as mere banditti.
It was said in the Senate at Paris, that France had chosen a ruler
from among a people whom the Romans would not take for their
slaves. “The Senator intended this remark as an insult to me,” said
the Emperor; “but he forgot how high a compliment he was thus
paying to the Corsicans. He spoke truly: the Romans never
purchased Corsican slaves: they knew that it was impossible to
reduce the Corsicans under the yoke of slavery.”
During the war for liberty in Corsica, some one proposed the singular
plan of cutting down and burning all the chesnut-trees, the fruit of
which furnishes sustenance to the mountaineers. By this means it
was hoped they would be compelled to descend to the plains to sue
for food and peace. Happily, said the Emperor, this was one of those
impracticable plans which can be realized only on paper. From very
different motives, Napoleon, during the early period of his life, had
constantly declaimed against the goats, which are very numerous in
the island, and commit great ravages among the trees. He wished
them to be entirely extirpated. On this subject he had some terrible
disputes with his uncle, Archdeacon Lucien, who possessed
numerous herds of goats, and who defended them like a patriarch.
In his rage, he reproached his nephew with being an innovator, and
inveighed against philosophic ideas, as the cause of the danger with
which his goats were threatened.
Paoli died in London at a very old age: he lived to see Napoleon First
Consul and Emperor. The Emperor expressed his regret at not having
recalled him. “That,” said he, “would have been highly gratifying to
me. Such an act would have been a real trophy of honour. But my
mind was absorbed in important affairs; I rarely had time to indulge
my personal feelings.”
After the Emperor’s return in 1815, when Lucien arrived in Paris,
Joseph advised the Emperor to appoint him Governor General of
Corsica. This measure was even determined on; the importance and
hurry of passing events alone prevented its execution. “If Lucien had
gone to Corsica,” said the Emperor, “he would still have remained
master of the Island, and what resources would it not have
presented to our persecuted patriots?—To how many unfortunate
families would not Corsica have afforded an asylum? He repeated
that he had perhaps committed a fault, at the time of his abdication,
in not reserving to himself the sovereignty of Corsica, together with
the possession of some millions of the civil list; and in not having
conveyed all his valuables to Toulon, whence nothing could have
impeded his passage. In Corsica, he would have found himself at
home; the whole population would have been, as it were, his own
family. He might have disposed of every arm and every heart. Thirty
thousand or even 50,000 allied troops could not have subdued him.”
No sovereign in Europe would have undertaken such a task. But it
was precisely the happy security of the situation that deterred him
from availing himself of it. He would not have it said that, amidst the
wreck of the French people, which he plainly foresaw, he alone had
been artful enough to gain the port.
Some one here observed that, according to the general opinion, he
might, in 1814, have secured the possession of Corsica instead of
the Island of Elba. “Certainly I might,” replied the Emperor, “and
those who are well acquainted with the affairs of Fontainebleau will
be surprised that I did not. I might then have reserved to myself
whatever I pleased. The humour of the moment led me to decide in
favour of Elba. Had I possessed Corsica, it is probable that my return
in 1815 would never have been thought of. Even at Elba, those
whose interest it was to keep me there decreed my return by their
own misgovernment and the non-fulfilment of the engagements
which they had entered into with me.”
We now reminded the Emperor of his intention of riding on
horseback; but he said that he would rather walk and chat. He
ordered his breakfast, after which we conversed for some time on
the old Court, the nobility who composed it, their pretensions, the
King’s equipages, &c.; and all this was compared with what the
Emperor had himself introduced.
The Emperor then reverted to the period of his Consulship, and
described the difficulties which he had experienced in forming the
kind of Court which was then kept up at the Tuileries. On his arrival
there, he was resolved to obliterate the recollection of the manners
and conflicts of the period to which he had just succeeded. But he
had hitherto passed his life in camps: he had just returned from
Egypt, and had quitted France when young and inexperienced. He
was a stranger to every one, and he at first found this a source of
great embarrassment. Lebrun acted as his guide during the first
years of his Consulship. Bankers and money-speculators were at that
time persons of the first consequence. No sooner did the Consul
enter upon his functions, than a host of these individuals crowded
round him, and eagerly offered to advance him considerable sums of
money. This conduct, though seemingly dictated only by generosity,
was not however without interested views. They were for the most
part men of bad character; and their offers were rejected. The First
Consul had a natural dislike of men of this profession. He said that
he had taken the firm determination to act upon different principles
from those of Scherer, Barras, and the Directory. He was anxious
that probity should become the main spring and feature of his new
government. The Consul was also immediately surrounded by the
wives of these money-lenders, who were all beautiful and elegant
women. Indeed a money-lender at that time seemed to regard it as
indispensably necessary that his wife should be a woman of
fascinating manners: it was a circumstance that tended materially to
assist his speculations. But the prudent Lebrun was at hand to direct
the young Telemachus. He resolved to exclude this sort of society
from the Tuileries. It was, however, no such easy matter to assemble
a suitable circle around the Consul: nobles were rejected, in order to
avoid giving offence to public opinion; and contractors were
excluded, with the view of purifying the morals of the new era.
These two classes being thus shut out, of course no very
distinguished society remained; and the Tuileries for some time
presented a sort of magic-lantern, very varied and changeable.
At Moscow, the Viceroy happened to meet with some letters written
by Princess Dolgoruki, who had been at Paris at the period here
alluded to. This correspondence gave a very favourable picture of
the Tuileries. The Princess observed that it was not precisely a Court,
nor yet exactly a camp; but something perfectly new in its kind. She
added that the First Consul did not carry his hat under his arm, nor
wear a dress-sword by his side; but that he was nevertheless a
swordsman. “However,” continued the Emperor, “such is the effect of
evil report that, owing to some such expressions as these having
been misrepresented to me, Princess Dolgoruki was very unjustly
treated. I ordered her, at that time, to quit France. We thought her
hostile to the principles of our government; but we were, as it may
be seen, mistaken. Madame G...., the mistress of M. de T...., for he
had not yet made her his wife, greatly contributed to alienate from
us the regard of the Russians.”
The Emperor observed that, on his return from Elba, he had
experienced far less embarrassment in composing his Court. “It was,
indeed,” said he, “all ready formed, by the ladies whom I termed my
widows. These were Madame Duroc, the Duchess of Istria,
Mesdames Regnier, Lagrand, and all the other widows of my first
generals. I told the Princesses, who consulted me on the method of
recomposing their Courts, to follow my example. Nothing was more
natural and proper. These ladies, though still young, were already
experienced in the world; and among them were several beautiful
and fascinating women. Most of them have now lost their fortunes;
some, I have been told, are re-married, and have changed their
names;[17] so that, of all the wealth and rank founded by me, no
traces will perhaps remain; even names will disappear. If this should
really be the case, will it not afford ground for saying that, after all,
there must have been a radical error in the selections I made. But it
will be the worse for the parties themselves; they will by this means
only furnish a triumph and a ground of insolence to the old
aristocracy.”
We again reminded the Emperor of his intended ride on horseback:
we urged him not to neglect it, because we knew it to be absolutely
necessary for his health. But we could not prevail on him to leave
the garden. “We are very well here,” said he; “we will have some
tents pitched on this spot.” We began to talk about the Faubourg St.
Germain, and the Hotel de Luynes, which the Emperor termed its
metropolis. He described to us the cause of the banishment of
Madame de Chevreuse. He said, he had frequently threatened to
visit her with this punishment, and for conduct of the most
mischievous and insolent nature. One day, when urged to the utmost
extremity, he addressed her as follows:—"Madam, according to the
feudal notions and doctrines, entertained by you and your friends,
you pretend to be the sovereigns of your estates! Now, on the same
principles, I may style myself the Sovereign Lord of France. I may
claim Paris as my village, and may banish from it every individual
who is obnoxious to me. I judge you by your own laws. Begone! and
never venture to return!" On decreeing her exile, the Emperor was
firmly resolved never to be prevailed on to recal her; because, he
said, he had endured much before he had decreed her punishment,
and he found himself compelled to set an example of severity to
spare the necessity of repeating it on others. This was one of his
grand principles.
I told the Emperor that I had frequently visited the Hotel de Luynes,
and that I had been well acquainted with Madame de Chevreuse and
her mother-in-law, for whom I had always entertained a great
regard. The latter had evinced singular and constant affection for
her daughter-in-law, having shared her exile, and accompanied her
in her different journeys from place to place. When proceeding on
my mission to Illyria, I one night met them both in an inn at the foot
of the Simplon. To be thus able to procure in the desert the most
trivial details relating to Paris and the Court, was to them a source of
unfeigned joy, and a most unexpected instance of good fortune.
They listened to me with no less eagerness than that evinced by
Fouquet on hearing the accounts of Lauzun. Their banishment from
the capital had been to them an absolute sentence of death; it had
overwhelmed them with despair!
Finally, I assured the Emperor that, for a considerable period, I had
observed the Hotel de Luynes, if not subdued, at least calmed and
reduced to something less than indifference; but our unexpected
disasters had revived its former spirit.
As to Madame de Chevreuse, who was a handsome, intelligent, and
amiable woman, with a somewhat romantic turn of mind, she had
doubtless been seduced by the charms of notoriety, or urged on by
her numerous flatterers and admirers, some of whom were very
unworthy of her regard. “I know it,” observed the Emperor; “she
hoped to recommence the Fronde; but I was not a minor Sovereign.”
The Musquito brig which left England on the 23rd of March, arrived
with files of the Journal des Debats down to the 5th of March, and
London papers to the 21st. On retiring to his closet, the Emperor
desired me to follow him. He began to peruse the Journal des
Debats; and, meanwhile, a letter was delivered to me from the
Grand Marshal. It had just arrived from Europe, and was addressed
to the Emperor. I handed it to him. He read it over once and sighed;
and, then, having read it a second time, he tore it, and threw the
fragments beneath the table. This letter was delivered open! The
Emperor then resumed his perusal of the Journals, and, suddenly
stopping, he said, after a few moments’ silence:—"That letter was
from poor Madame: she is well, and wishes to come to reside with
me at St. Helena!" After this he continued his reading. This, which
was the first letter that the Emperor had received from any
individual of his family, was in the handwriting of Cardinal Fesch. The
Emperor was evidently much hurt by its having been delivered to
him open.

MOREAU, GEORGES, AND PICHEGRU.—DIFFERENCE OF OPINION PRODUCED BY

THEIR CONSPIRACY IN THE CAMP OF BOULOGNE AND IN PARIS.
30th.—The Emperor went out about two o’clock, and we all attended
him. He began to converse about the intelligence contained in the
French papers which he had just received, and alluded to the statues
which, it was stated, were to be erected to the memory of Moreau
and Pichegru. “A statue to Moreau,” said he, “whose conspiracy in
1803 is now so well proved! Moreau, who, in 1813, died fighting
under the Russian standard! A monument to the memory of
Pichegru, who was guilty of one of the most heinous of crimes! who
purposely suffered himself to be defeated, and who connived with
the enemy in the slaughter of his own troops! And after all,”
continued he, “history is only made up of reports which gain credit
by repetition. Because it has been repeatedly affirmed that these
were great men, who deserved well of their country, they will at
length pass for such, and their adversaries will be despised.”
Some one present remarked that it might have been thus in the dark
ages of ignorance; but that now the multitude of monuments and
public documents, the arts of printing and engraving, and the
general diffusion of knowledge, must always render truth accessible
to those who wish to come at it; and, as each party has its own
historians, the thinking reader will always be enabled to form an
impartial opinion.
The Emperor then described at length the affairs of Moreau,
Georges, and Pichegru, to which I have before alluded, and of which
I promised further details. He now informed us that the man who
made the first confessions indicated, though without naming him, a
person to whom Georges and the other leaders of the conspiracy
never spoke without taking off their hats, and whom they treated
with the utmost consideration and respect. It was at first supposed
that this individual must have been the Duke de Berri; and some
concluded him to have been the Duke d’Enghien, during his
momentary appearance. Charles d’Hosier, one of the conspirators,
unexpectedly drew aside the veil. A few days after his arrest, he was
seized with a fit of melancholy and hanged himself in prison. The
alarm was however given, and he was cut down. Stretched on his
bed, and while yet struggling between life and death, he vented
repeated imprecations against Moreau, and accused him of having
treacherously seduced many well-disposed men, and held out to
them promises of assistance which he never realized. He likewise
mentioned the names of Georges and Pichegru. This was the first
circumstance that excited suspicion against Georges and Pichegru;
there was previously no idea of either the one or the other having
been engaged in the conspiracy. Real, who had hastened to this sort
of death-bed confession of d’Hosier, proposed to the Consul that he
should order the arrest of Moreau.
“This event created a great sensation,” said the Emperor. “The public
mind was wrought up to a high pitch of fermentation. Doubts were
entertained of the truth of the statements made by the Government
respecting the extent of the conspiracy and the number of the
conspirators. Of the latter it was affirmed there were about forty in
Paris. Their names were published, and the First Consul pledged his
honour to secure them. He summoned Bassières, and gave orders
that he, with his corps, should surround and guard the walls of Paris.
For the space of six weeks, nobody was suffered to quit the capital
without special permission. A general gloom prevailed through Paris;
but every day the Moniteur announced the arrest of one or two of
the individuals who it was alleged were concerned in the conspiracy.
Public opinion took a turn in my favour; and indignation against the
conspirators increased in proportion as they were secured. Not one
escaped.”
The public papers of the period detail the particulars of the arrest of
Georges, who killed two men before he could be secured. It appears
that he was betrayed by his comrade, who drove the cabriolet in
which they were both riding together.
As to Pichegru, he was the victim of the basest treachery. “This
circumstance,” said the Emperor, “was truly a disgrace to human
nature. He was sold by his intimate friend; by a man whom I will not
name, on account of the horror and disgust which his conduct is
calculated to excite.” We informed the Emperor that the name of this
individual had been mentioned in the Moniteur, at which he
expressed surprise. “This man,” continued he, "who was formerly a
military officer, and who has since followed the business of a
merchant at Lyons, offered to deliver up Pichegru for 100,000
crowns. On the day on which he made this proposal, he stated that
they had, on the preceding evening, supped together, and that
Pichegru, finding himself every day alluded to in the Moniteur, and
being aware that the critical moment was fast approaching, said, ‘If I
and a few other Generals were boldly to present ourselves to the
troops, should we not gain them over?’—‘No,’ replied the friend, ‘you
form a wrong idea of the state of feeling in France; you would not
gain over a single soldier.’—He spoke truly. At night, the faithless
friend conducted the officers of the police to Pichegru’s door; and he
gave them a minute description of his chamber and his means of
defending himself. Pichegru had pistols on his bed-room table, and
he kept a light burning while he slept. The officers gently unlocked
the door by means of false keys, which the treacherous friend had
procured for them. The table was overturned, the candle was
extinguished, and the officers seized Pichegru, who immediately
jumped out of bed. He was a very powerful man; he struggled
desperately, and it was found necessary to bind him and convey him
to prison, without waiting till he could be dressed."
On being placed at the head of the government, the First Consul was
extremely anxious to tranquillize the western departments. He
summoned nearly all the leading men of those districts, and
succeeded in rousing several of them to a sense of the interests and
glory of their country; he added that he even drew tears from the
eyes of some. Georges had his turn among the rest. The Emperor
said that he had endeavoured to touch every individual string of his
heart; but in vain, he could produce no vibration. He found him lost
to every generous feeling, and coldly intent on his own ambitious
calculations. He persisted in his determination to command his
Cantons. The Consul, having exhausted every conciliatory argument,
at length assumed the language of the first Magistrate of France. He
dismissed him, and recommended him to go home and live quietly
and submissively; and above all, not to mistake the nature of the
course he had that moment adopted, nor to attribute to weakness
what was only the result of his moderation and the consciousness of
his power. He desired him to repeat to himself, and to all who were
connected with him, that, so long as the First Consul should hold the
reins of authority, there would be no chance of safety for any who
might dare to engage in conspiracy. Georges took his leave; but, as
the event proved, not without having imbibed from this conference a
feeling of respect for Napoleon, on whose destruction, however, he
still continued bent.
Moreau was the rallying point and the centre of attraction to the
conspirators, who came from London to attack Paris. It appeared
that Lajollais, his Aide-de-camp, had deceived these men, by
addressing them in the name of Moreau, and telling them that that
General was secure of popular favour throughout the whole of
France, and could dispose of the whole army. Moreau constantly
assured them that he could command no one, not even his Aide-de-
camp; but that if they killed the First Consul, they might do any
thing.
Moreau, when left to himself, was a very good sort of man. He was
easily led, and this accounts for his inconsistencies. He left the
palace in raptures, and returned to it full of spleen and malice;—
having in the interim seen his mother-in-law and his wife. The First
Consul, who would have been very glad to have gained him over to
his side, once made it up with him completely; but their friendship
lasted only four days. The Consul then vowed that he would never
renew it. In fact, attempts were afterwards frequently made to
reconcile them; but Napoleon never would agree to it. He foresaw
that Moreau would commit some fault, that he would lose himself;
and certainly he could not have done so in a way more
advantageous to the First Consul.
Some days previous to the battle of Leipsic, some carriages
containing property and papers belonging to Moreau, which were on
their way to his widow in England, were intercepted at Wittemberg.
Among those papers, there was a letter from Madame Moreau
herself, in which she advised her husband to lay aside his silly
wavering conduct, and to come boldly to a determination. She urged
him to assist in the triumph of the legitimate cause, that of the
Bourbons. In answer to this, Moreau wrote a few days before his
death, begging her not to trouble him with her chimeras. “I have
come near enough to France,” said he, "to learn all that is going
forward there. I have got into a real hornet’s nest."
The Emperor was on the point of publishing these intercepted
papers in the Moniteur; but there still existed in France some
persons blindly tenacious of the opinion they had always maintained
respecting Moreau, and who persisted in regarding him as a victim
of tyranny. The counter-revolution had not yet afforded an
opportunity of making known those acts hitherto disavowed, and of
claiming their recompense. The circumstance of personal enmity
prevented the Emperor from executing his intention. He thought that
it would not be becoming to revive this enmity for his own
advantage, and to tarnish the memory of a man who had just fallen
on the field of battle.
The trial of Moreau and Pichegru, which was protracted for such a
length of time, violently agitated the public mind. What added to the
notoriety and interest of this trial was its connection with the affair
of the Duke d’Enghien, with which it became interwoven. “I have,”
said the Emperor, “been reproached with having committed a great
fault in that trial. It has been compared with the affair of the
necklace, in the reign of Louis XVI., which that Monarch put into the
hands of Parliament, instead of having it judged by a Commission.
Politicians have affirmed that I should have contented myself with
consigning the criminals to the judgment of a Military Commission. It
would have been ended in eight and forty hours. I could have done
it; it was legal, and nothing more would have been required of me; I
should have avoided the risks to which I was exposed. But I felt my
power so unlimited, and I was at the same time so strong in the
justice of my cause, that I was determined the affair should be open
to the observation of the whole world. For this reason the
ambassadors and agents of Foreign powers were present during the
proceedings!”
One of the company present here observed to the Emperor that the
course he then adopted had proved advantageous to history and
honourable to his own character. It had furnished three volumes of
authentic documents relating to the trial.
Another individual of the Emperor’s suite, who, at the time of this
celebrated trial, was with the army at Boulogne, said that all these
events, even the affair of the Duke d’Enghien, had there excited but
little interest, and that, on his return to Paris, some time afterwards,
he was astonished to observe the sensation which they had created
in the capital.
The Emperor remarked that the public mind had indeed been highly
excited, particularly on the occasion of the death of the Duke
d’Enghien, which event, he said, still appeared to be judged of in
Europe with blindness and prejudice. He maintained his right of
adopting the step he had taken, and enumerated the reasons which
had urged him to it. He then adverted to the many attempts that
had been made to assassinate him, and observed that he was bound
in justice to say that he had never detected Louis XVIII. in any direct
conspiracy against his life, though such plots had been incessantly
renewed in other quarters. With regard to that Prince he had heard
only of his systematic plans, ideal operations, &c.
“If,” continued he, “I had continued in France in 1815, I intended to
have given publicity to some of the later attempts that were made
against me. The Maubreuil affair, in particular, should have been
solemnly investigated by the first Court of the Empire, and Europe
would have shuddered to see to what an extent the crime of secret
assassination could be carried.”

CONVERSATION RESPECTING THE SITUATION OF ENGLAND.—LETTERS

DETAINED BY THE GOVERNOR.—CHARACTERISTIC OBSERVATIONS.
31st.—At five o’clock, I went to join the Emperor in the garden; we
were all assembled there. The conversation turned on politics. He
described the melancholy situation of England, amidst her triumphs.
He alluded to the immensity of her debt, the madness, the
impossibility of her becoming a continental power, the dangers which
assailed her constitution, the embarrassment of her ministers, and
the just clamour of the people. England with her 150 or 200
thousand men, made as many efforts as he, the Emperor, had ever
made during the period of his great power, and perhaps even more.
He had never employed beyond 500 thousand French troops. The
traces of his Continental system were followed by all the powers on
the Continent, and would be pursued still further in proportion as
those powers became more settled. He did not hesitate to say, and
he proved it, that England would have gained by adhering to the
treaty of Amiens; that such a line of conduct would have been to the
advantage of all Europe, but that Napoleon himself, and his glory
would have suffered by it. Yet it was England, and not he, who broke
the treaty.
There was only one course, he continued, for England to pursue;
namely, to return to her constitution and abandon the military
system; to interfere with the Continent only through her maritime
influence, in which she was pre-eminent. It was, he said, easy to
foresee that great calamities would assail her should she adopt any
other course, and this she would inevitably do, because all her
aristocracy urged her to it, and because the folly, pride, or venality
of her present ministry caused her to persist in the system she was
pursuing.
The conversation being concluded, the Emperor returned to his
study, and desired me to follow him. He told me that a letter which
had been sent to him from England by post was said to have been
kept back by the Governor, because it was not addressed to him
officially; and it was said that a letter for the Grand Marshal had
been detained for the same reason. The Emperor observed that, if
this were true, there was something peculiarly cruel in the conduct
of the Governor, in having sent back the letters without even
mentioning them to us, and without affording us the consolation of
knowing from whom they came.... A neglect of form, he said, might
easily be corrected in the Island; but it could not so easily be
observed at 2000 leagues’ distance. I told the Emperor that a
circumstance nearly similar to that which he had just mentioned had
occurred to me eight or ten days back. “A person who was on his
way to Europe had tormented me with his offers of service. I yielded
to his solicitations, and commissioned him to order me some shoes
and to get a watch changed for me, for there is no person here who
knows how to repair a watch. The Governor had forbidden the
execution of those commissions, because they had not been
addressed to himself. I have said nothing on the subject to any one,
Sire, because it is a principle with me to conceal an insult for which I
cannot obtain redress; but I shall find an opportunity to tell the
Governor my mind. In the mean time, neither he nor the person to
whom I gave the commission, has been able to draw from me a line,
or a single word, though the latter has made several attempts to do
so.”
After dinner the Emperor, conversing on our situation and the
conduct of the Governor, who came to-day and took a rapid circuit
round Longwood, reverted to the subject of the last interview they
had had together, and made some striking observations respecting
it. “I behaved very ill to him, no doubt,” said he, “and nothing but
my present situation could excuse me; but I was out of humour, and
could not help it; I should blush for it in any other situation. Had
such a scene taken place at the Tuileries, I should have felt myself
bound in conscience to make some atonement. Never, during the
period of my power, did I speak harshly to any one without
afterwards saying something to make amends for it. But here I
uttered not a syllable of conciliation, and I had no wish to do so.
However, the Governor proved himself very insensible to my
severity; his delicacy did not seem wounded by it. I should have
liked, for his sake, to have seen him shew a little anger, or bang the
door after him when he went away. This would at least have shown
that there was some spring and elasticity about him; but I found
nothing of the kind.”
The Emperor then again resumed his conversation on political
affairs, which he maintained with so much spirit and interest, that I
could have forgotten for a time what part of the world I was in. I
could have believed myself still at the Tuileries or in the Rue de
Bourgogne.